# IMMUNE MECHANISMS IN EXPERIMENTAL SYPHILIS

> **NIH NIH R01** · UNIVERSITY OF CALIFORNIA LOS ANGELES · 1991 · $206,802

## Abstract

DESCRIPTION:  (Adapted from applicant's abstract) While immune serum
antibody has been shown to inhibit Treponema pallidum subsp.  pallidum
adherence and invasion of host cell monolayers, augment macrophage
phagocytosis of treponemes, and kill treponemes in the presence of
complement, the relationship of these potential immune mechanisms to the
contribution of protective immunity during syphilitic infection has not
been established.  Using a novel in vitro killing assay developed in the
investigator's laboratory, they have demonstrated that T. pallidum binds
immune serum antibody within 30 minutes; this bound antibody inhibits
treponemal adherence and invasion and has treponemicidal potential.  This
assay has shown that the slow kinetics of killing are determined by the
rate of complement activation and correlate with the aggregation of T.
pallidum rare outer membrane protein (TROMP), molecules that the
investigator has recently identified by freeze-fracture analysis and that
are likely to represent the initial surface exposed targets on this
organism.  Further, the investigator has shown that treponemicidal activity
measured by this assay correlates with the ontogeny of immunity to
symptomatic and disseminated infection in experimental rabbit syphilis.
Strategies are proposed in this study to use this novel in vitro assay
system in combination with experimentally infected rabbits to relate
directly complement-dependent treponemicidal activity to TROMP and
treponemal adherence and invasion inhibition to the status of immunity
during the course of experimental rabbit syphilis.  The specific aims of
this study are:  1) relate the ontogeny of immunity in experiment rabbit
syphilis and the development of treponemicidal antibody to tROMP, 2)
determine the mechanism(s) of antibody-mediated, complement-dependent, in
vitro treponemicidal activity, and 3) relate the development of immunity in
experimental rabbit syphilis to the inhibition of treponemal adherence and
invasion of host cells.  It is believed that the results of this study will
provide a further understanding of the specific immune mechanisms
responsible for acquired resistance against syphilis.

## Key facts

- **NIH application ID:** 3125233
- **Project number:** 2R01AI012601-15
- **Recipient organization:** UNIVERSITY OF CALIFORNIA LOS ANGELES
- **SAM.gov UEI:** RN64EPNH8JC6
- **Principal Investigator:** JAMES Nathaniel MILLER
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1991
- **Award amount:** $206,802
- **Award type:** 2
- **Project period:** 1978-06-01 → 1994-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3125233

## Citation

> US National Institutes of Health, RePORTER application 3125233, IMMUNE MECHANISMS IN EXPERIMENTAL SYPHILIS (2R01AI012601-15). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3125233. Licensed CC0.

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